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Physiological Functions and Pathological Effects of Microglia
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Physiological Functions and Pathological Effects of Microglia

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 20 September 2025 | Viewed by 1457

Special Issue Editor

Prof. Dr. Hiroshi Nakanishi

E-Mail Website
Guest Editor
Department of Pharmacology, Faculty of Pharmacy, Yasuda Women’s University, Yasuhigashi, Hiroshima 731-0153, Japan
Interests: microglia; brain inflammation; cathepsins; Alzheimer’s disease; Porphyromonas gingivalis

Special Issue Information

Dear Colleagues,

Microglia comprise a variety of subsets with multiple roles in the healthy and diseased brain. Microglia engulf dendritic spines and prune connections between neurons to establish mature patterns of connection during postnatal development. On the other hand, a fault in synaptic elimination and disturbance of the microglial circadian clock system are accepted characteristic abnormalities in neuropsychiatric disorders, including autism. Furthermore, excessive inflammatory and immune responses mediated by pathological microglia are involved in the pathogenesis of neurodegenerative diseases, including Alzheimer’s disease. Therefore, in this Special Issue, we aim to retrieve the bank of data on physiological functions and pathological effects of microglia, which may aid in gaining a better understanding of their emergent properties in the brain.

Prof. Dr. Hiroshi Nakanishi
Guest Editor

Manuscript Submission Information

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Keywords

  • circadian clock
  • homeostasis
  • immune response
  • microglia
  • neurodegenerative diseases
  • neuroinflammation
  • neuropsychiatric disorders
  • neuromodulation
  • phagocytosis
  • synaptic pruning

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Published Papers (2 papers)

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Research

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17 pages, 3942 KiB  
Article
Noradrenaline Synergistically Enhances Porphyromonas gingivalis LPS and OMV-Induced Interleukin-1β Production in BV-2 Microglia Through Differential Mechanisms
by Sakura Muramoto, Sachi Shimizu, Sumika Shirakawa, Honoka Ikeda, Sayaka Miyamoto, Misato Jo, Uzuki Takemori, Chiharu Morimoto, Zhou Wu, Hidetoshi Tozaki-Saitoh, Kosuke Oda, Erika Inoue, Saori Nonaka and Hiroshi Nakanishi
Int. J. Mol. Sci. 2025, 26(6), 2660; https://doi.org/10.3390/ijms26062660 - 15 Mar 2025
Viewed by 673
Abstract
Infection with Porphyromonas gingivalis (Pg), which is a major periodontal pathogen, causes a large number of systemic diseases based on chronic inflammation such as diabetes and Alzheimer’s disease (AD). However, it is not yet fully understood how Pg can augment local [...] Read more.
Infection with Porphyromonas gingivalis (Pg), which is a major periodontal pathogen, causes a large number of systemic diseases based on chronic inflammation such as diabetes and Alzheimer’s disease (AD). However, it is not yet fully understood how Pg can augment local systemic immune and inflammatory responses during progression of AD. There is a strong association between depression and elevated levels of inflammation. Noradrenaline (NA) is a key neurotransmitter that modulates microglial activation during stress conditions. In this study, we have thus investigated the regulatory mechanisms of NA on the production of interleukin-1β (IL-1β) by microglia following stimulation with Pg virulence factors, lipopolysaccharide (LPS), and outer membrane vesicles (OMVs). NA (30–1000 nM) significantly enhanced the mRNA level, promoter activity, and protein level of IL-1β up to 20-fold in BV-2 microglia following treatment with Pg LPS (10 μg/mL) and OMVs (150 μg of protein/mL) in a dose-dependent manner. Pharmacological studies have suggested that NA synergistically augments the responses induced by Pg LPS and OMVs through different mechanisms. AP-1 is activated by the β2 adrenergic receptor (Aβ2R)-mediated pathway. NF-κB, which is activated by the Pg LPS/toll-like receptor 2-mediated pathway, is required for the synergistic effect of NA on the Pg LPS-induced IL-1β production by BV-2 microglia. Co-immunoprecipitation combined with Western blotting and the structural models generated by AlphaFold2 suggested that cross-coupling of NF-κB p65 and AP-1 c-Fos transcription factors enhances the binding of NF-κB p65 to the IκB site, resulting in the synergistic augmentation of the IL-1β promoter activity. In contrast, OMVs were phagocytosed by BV-2 microglia and then activated the TLR9/p52/RelB-mediated pathway. The Aβ2R/Epac-mediated pathway, which promotes phagosome maturation, may be responsible for the synergistic effect of NA on the OMV-induced production of IL-1β in BV-2 microglia. Our study provides the first evidence that NA synergistically enhances the production of IL-1β in response to Pg LPS and OMVs through distinct mechanisms. Full article
(This article belongs to the Special Issue Physiological Functions and Pathological Effects of Microglia)
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Review

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21 pages, 1045 KiB  
Review
Microglia/Macrophages in Autoimmune Demyelinating Encephalomyelitis (Multiple Sclerosis/Neuromyelitis Optica)
by Ryo Yamasaki
Int. J. Mol. Sci. 2025, 26(8), 3585; https://doi.org/10.3390/ijms26083585 - 10 Apr 2025
Viewed by 351
Abstract
Microglia and macrophages are critical mediators of immune responses in the central nervous system. Their roles range from homeostatic maintenance to the pathogenesis of autoimmune demyelinating diseases such as multiple sclerosis and neuromyelitis optica spectrum disorder. This review explores the origins of microglia [...] Read more.
Microglia and macrophages are critical mediators of immune responses in the central nervous system. Their roles range from homeostatic maintenance to the pathogenesis of autoimmune demyelinating diseases such as multiple sclerosis and neuromyelitis optica spectrum disorder. This review explores the origins of microglia and macrophages, as well as their mechanisms of activation, interactions with other neural cells, and contributions to disease progression and repair processes. It also highlights the translational relevance of insights gained from animal models and the therapeutic potential of targeting microglial and macrophage activity in multiple sclerosis and neuromyelitis optica spectrum disorder. Full article
(This article belongs to the Special Issue Physiological Functions and Pathological Effects of Microglia)
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